Evidence map›Paper›PMID 40990917›Full record

ArticleeLife2025

Ubiquitination-activated TAB-TAK1-IKK-NF-κB axis modulates gene expression for cell survival in the lysosomal damage response.

Akinori Endo, Chikage Takahashi, Naoko Ishibashi, Yasumasa Nishito, Koji Yamano, Keiji Tanaka, Yukiko Yoshida

Abstract read
In one paragraph

Article in eLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. [Ubiquitination-mediated regulation of T cell homeostasis and autoimmune diseases].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
    Review
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Akinori EndoLaboratory of Protein Metabolism, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.ORCID https://orcid.org/0000-0003-0225-4832
Chikage TakahashiLaboratory of Protein Metabolism, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Naoko IshibashiLaboratory of Protein Metabolism, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Yasumasa NishitoTechnology Research Division, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Koji YamanoIntracellular Quality Control Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.ORCID https://orcid.org/0000-0002-4692-161X
Keiji TanakaLaboratory of Protein Metabolism, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Yukiko YoshidaLaboratory of Protein Metabolism, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.ORCID https://orcid.org/0000-0002-0629-0219

Funding

Japan Agency for Medical Research and Development JP21gm6410012Japan Agency for Medical Research and Development JP24gm14100003Japan Society for the Promotion of Science JP18K14623Japan Society for the Promotion of Science JP20K06568Japan Society for the Promotion of Science JP22H02305Japan Society for the Promotion of Science JP23H04921Japan Society for the Promotion of Science JP23H04923Japan Society for the Promotion of Science JP23K23841
6 · The paper itself

Abstract

The lysosomal damage response is important for the maintenance of cellular homeostasis in human cells. Although the mechanisms underlying the repair and autophagic elimination of damaged lysosomes have been elucidated, the early signal transduction pathways and genes induced in response to lysosomal damage remain elusive. We performed transcriptome and proteome analyses and found that the TAB-TAK1-IKK-NF-κB axis is activated by K63-linked ubiquitin chains that accumulate on damaged lysosomes. This activates the expression of various transcription factors and cytokines that promote anti-apoptosis and intercellular signaling. The findings highlight the crucial role of ubiquitin-regulated signal transduction and gene expression in cell survival and cell-cell communication in response to lysosomal damage. The results suggest that the ubiquitin system is not only involved in the removal of damaged lysosomes by lysophagy, but also functions in the activation of cellular signaling for cell survival.

Indexed as

Gene Expression RegulationI-kappa B KinaseLysosomesMAP Kinase Kinase KinasesNF-kappa BUbiquitinationCell SurvivalHumansMAP Kinase Kinase Kinase 7Signal TransductionI-kappa B KinaseMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesNF-kappa Bcell biologyhumanlysosomal damage responseNF-κBTABTAK1ubiquitin

Identifiers

PMID40990917
PMCPMC12459955

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.